Autoimmune reaction and type 2 diabetes linked in breakthrough study

This is HUGE!!
http://www.diabetes.co.uk/news/2011/Apr/autoimmune-reaction-and-typ...

"Scientists at the Stanford University School of Medicine and the University of Toronto have showed that type 2 diabetes could derive from an autoimmune reaction from within the body. It is hoped the breakthrough will lead to new therapies for treating the condition."

One of the study authors stated:
"This work will change the way people think about obesity, and will likely impact medicine for years to come as physicians begin to switch their focus to immune-modulating treatments for type 2 diabetes."

I can't help but be amazed at how much we continue to learn about all types of diabetes...

Tags: autoimmune, study, type2

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Wow, yes we do! Long story short:
As a child, I was sick a lot. Weird assortment of illnesses. Bouts of bronchitis, allergies, joint problems, severe headaches, nose bleeds, extreme fatigue (often mistake for laziness), and collapsing for no apparent reason. Lost a baby in '92, diagnosed with Lupus, later on with degenerative disc disorder, diabetes, high blood pressure, and now wheat and dairy flare up my allergies and asthma. I'm 47, but feel like I'm 74... I've often believed it was thyroid related, but no insurance means I can believe all I want, but the most I can hope for is to keep things under control for during flare ups or segments of time when we can afford the doctor visits & meds. (I have boys too! 4 boys: 22, 21, 17 & 15.
manny:

no offense - like your optimism; and yes science needs to do the research even if it is all over the field and on esoteric items.

But - folks eyes, kidneys, limbs are rotting out still while this research grinds on.
Halting, slowing the rot would be a first great step. What is insulin resistance and what causes it and reseraching it in depth would be great first step.

Type 2 diabetes insulin resistance is not a uniform monolithis disease.

Cure seems to suggest that one will be able to eat anything even in face of following constrints:

Human body relies upon a storage hormone insulin to regulate body BG by routing excess glucose from blood stream to storage resources of liver, fat cells and skeletal muscle cells.

If those cells are filled up based upon constant high levels of calorie/energy input and constantly low levels of exercise - energy burn, its hard to understand how a body can maintain BG levels at safe lower levels.

The old Hunter gatherer gene set/gut/intestine were optimized years ago - for as a friend of mine says - a control engineer to bump along the bottom of food supply and periods of starvation and scrawny food.

As the current human body as best as I can tell was not optimized - organized to thow over the side excess calorie input and instead grabs all calories regardless of how levels of glucose storage are at in the body resulting in the necessity of calorie input management as well as energy burn sufficient to keep energy balance near zero will be part of that final solution.

Like you, I also want a cure. So far as best as I can tell Type 1 lends itself to the cure you are describing. I believe that is 18 to 20 % of all diabetics. The balance are type 2.

Yes, in the end, maybe genes are at fault but without majjor design changes - replumbing of a type 2 Insulin Resistant Diabetics genes, gut/intestine operation; I am unclear how we make progess on the front you describe.
Meanwhile - excessive liver glucose release goes ignored as a major cause of diabetes:

Pitt team identifies key protein causing excess liver production of glucose in diabetes
PITTSBURGH, Sept. 28 – Researchers at the John G. Rangos Sr. Research Center at Children's Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine have identified a powerful molecular pathway that regulates the liver's management of insulin and new glucose production, which could lead to new therapies for diabetes. The findings were published online this week in Diabetes, a journal of the American Diabetes Association.

Usually, the liver stores excess blood sugar as glycogen, which it doles out overnight during sleep and other periods of fasting to keep glucose levels within a normal physiological range, explained H. Henry Dong, Ph.D., associate professor of pediatrics, Pitt School of Medicine. But in diabetes, the liver continues to pump out glucose even when insulin is provided as a treatment.

"Scientists have been trying to find the factors that contribute to this liver overproduction of glucose for decades," Dr. Dong said. "If we can control that pathway, we should be able to help reduce the abnormally high blood sugar levels seen in patients with diabetes."

He and his team have been studying a family of proteins called Forkhead box or FOX, and for the current project focused on one called FOX06. They found that mice engineered to make too much FOX06 developed signs of metabolic syndrome, the precursor to diabetes, including high blood sugar and high insulin levels during fasting as well as impaired glucose tolerance, while mice that made too little FOX06 had abnormally low blood sugars during fasting.

"In a normal animal, a glucose injection causes blood sugar level to rise initially and then it goes back to normal range within two hours," Dr. Dong said. "In animals that made too much FOX06, blood sugar after a glucose injection doesn't normalize within two hours. They have lost the ability to regulate the level while the liver keeps making unneeded glucose."

Other experiments showed that diabetic mice have abnormally high levels of FOX06 in the liver, he added. Blocking the protein markedly reduced liver production of glucose, although blood sugar did not completely normalize. Within two weeks of treatment, there was significant improvement in blood sugar and glucose metabolism in diabetic mice.

Tests with human liver cells echoed the importance of FOX06's role in glucose production.

"These findings strongly suggest that FOX06 has potential to be developed as a therapeutic target," Dr. Dong said. "If we can inhibit its activity, we can possibly slow the liver's production of glucose in patients with diabetes and better control blood sugar levels."


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Co-authors include lead author Dae Hyun Kim, Ph.D., and other researchers from the University of Pittsburgh's departments of Pediatrics and of Pathology. The study was funded by the National Institutes of Health.

About the University of Pittsburgh School of Medicine

As one of the nation's leading academic centers for biomedical research, the University of Pittsburgh School of Medicine integrates advanced technology with basic science across a broad range of disciplines in a continuous quest to harness the power of new knowledge and improve the human condition. Driven mainly by the School of Medicine and its affiliates, Pitt has ranked among the top 10 recipients of funding from the National Institutes of Health since 1997.

Likewise, the School of Medicine is equally committed to advancing the quality and strength of its medical and graduate education programs, for which it is recognized as an innovative leader, and to training highly skilled, compassionate clinicians and creative scientists well-equipped to engage in world-class research. The School of Medicine is the academic partner of UPMC, which has collaborated with the University to raise the standard of medical excellence in Pittsburgh and to position health care as a driving force behind the region's economy. For more information about the School of Medicine, see www.medschool.pitt.edu.

About Children's Hospital of Pittsburgh of UPMC

Renowned for its outstanding clinical services, research programs and medical education, Children's Hospital of Pittsburgh of UPMC has helped establish the standards of excellence in pediatric care. From Ambulatory Care to Transplantation and Cardiac Care, talented and committed pediatric experts care for infants, children and adolescents who make more than 1,000,000 visits to Children's, its many neighborhood locations, and Children's Community Pediatrics practices each year.

Children's also consistently has been named to several elite lists of pediatric health care facilities, including U.S. News & World Report's Honor Roll of America's "Best Children's Hsopitals" and the Leapfrog Group. Also, Pediatric research programs at Children's Hospital and the University of Pittsburgh School of Medicine ranked eighth in number of grants from the NIH for fiscal year 2010.





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Here is excellent summary and text dealing with Insulin Resistance and T2 and work done doing studies on skeletal muscle cells and mag resonance spectography looking at glycon storage levels.

Very interesting.
Attachments:

Old thread, but if you're interested, here is a link that talks more about it:

http://med.stanford.edu/ism/2011/april/engleman.html

Or you can Google Stanford University Type 2 Diabetes Autoimmunity, and get a whole raft of articles.

To those of you who are concerned about other issues, like what about the folks who aren't overweight or obese, I'd like to remind you that T2 is a GARBAGE CAN diagnosis -- anyone who doesn't have the classic T1 antibodies is, by definition, T2, but that doesn't mean they all have the same disease. Those who ARE obese, and have metabolic syndrome and are demonstrably insulin-resistant, fit what I call "classic T2" (NO blame intended!), but there are a significant number, although a minority, of people who are called T2 but who DON'T have the classic disease. No one has actually described what these people have (excluding those who actually have LADA or MODY), so I have called it Type Weird for many years.

The term "Thin T2" is a bad one, because it points doctors' thinking in the wrong direction -- right straight towards insulin resistance and weight loss, when that might not be the problem at all. But the fact is that NO ONE knows what the problem is. If you want to talk about an orphan disease, you guys are IT. That's why I like Type Weird -- at least I'M acknowledging that you're NOT classic T1, nor classic T2, nor MODY nor LADA if you've been tested for them. Wish I was a scientist and wish I had the funds to research it!

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